title: Myocardial deformation and twist mechanics in adults with metabolic syndrome: impact of cumulative metabolic burden.
abstract: OBJECTIVE
  The aim of the study is to characterize left ventricular (LV) myocardial mechanics in adults with metabolic syndrome (MetS), and elucidate the effects of multiple risk-factors on myocardial function using speckle tracking echocardiography (STE); a more sensitive method than conventional echocardiography for detecting subclinical myocardial dysfunction.
  
  
  METHODS
  Cross-sectional analyses of 92 adults (50-70 years) with MetS, and 50 healthy controls included conventional echocardiography, blood biochemistry, and STE-derived myocardial longitudinal, circumferential, and twist mechanics.
  
  
  RESULTS
  Using conventional measures, MetS participants revealed LV hypertrophy and reduced diastolic function compared with controls, while systolic function was preserved. From STE, MetS participants showed attenuated longitudinal strain (-16.8% ± 2.8% vs. -20.6% ± 2.7%), and both diastolic (1.1 ± 0.2 vs. 1.4 ± 0.3 s s(-1) ) and systolic (-1.0 ± 0.1 vs. -1.2 ± 0.2 s s(-1) ) strain rate (SR). Circumferential strain, SR, and twist mechanics did not differ. Participants with the highest number of MetS factors or diabetes demonstrated the greatest reduction in longitudinal strain and SR. Abdominal obesity, TNF-α, HbA1c , and systolic dyssynchrony explained 48% of impairment in longitudinal strain.
  
  
  CONCLUSIONS
  Impaired longitudinal myocardial diastolic and systolic function, but preserved circumferential function and twist mechanics were found in MetS participants, indicative of altered subendocardial function. This dysfunction was best predicted by abdominal obesity, inflammation, glucose-intolerance, and systolic dyssynchrony.
authors.affiliation: Avignon University, LAPEC EA4278, Avignon, France; School of Exercise Science, Australian Catholic University, Melbourne, Australia.
authors.forename: Edward
authors.initials: E
authors.lastname: Crendal
authors.forename: Guillaume
authors.initials: G
authors.lastname: Walther
authors.forename: Agnes
authors.initials: A
authors.lastname: Vinet
authors.forename: Frédéric
authors.initials: F
authors.lastname: Dutheil
authors.forename: Geraldine
authors.initials: G
authors.lastname: Naughton
authors.forename: Bruno
authors.initials: B
authors.lastname: Lesourd
authors.forename: Robert
authors.initials: R
authors.lastname: Chapier
authors.forename: Thomas
authors.initials: T
authors.lastname: Rupp
authors.forename: Daniel
authors.initials: D
authors.lastname: Courteix
authors.forename: Philippe
authors.initials: P
authors.lastname: Obert
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology; D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D009765:Obesity / Q000150:complications / Q000503:physiopathology; D013599:Systole / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D006442:Glycated Hemoglobin; D014409:Tumor Necrosis Factor-alpha; C517652:hemoglobin A1c protein, human